Evidence map›Paper›PMID 39741520›Full record

ReviewFrontiers in aging neuroscience2024

Mitochondrial dysfunction and Alzheimer's disease: pathogenesis of mitochondrial transfer.

Yun Wei, Xinlei Du, Hongling Guo, Jingjing Han, Meixia Liu

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in aging neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

  1. Article
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  4. The role of mitochondrial Na⁺/Ca²⁺ exchanger in brain cell aging.Journal of bioenergetics and biomembranes · 2026
    Review
  5. Review
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  7. Review
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  9. Review
  10. Article
  11. Interplay Between 3D Chromatin Architecture and Gene Regulation at theInternational journal of molecular sciences · 2025
    Article
  12. Review
  13. Article
  14. Stem cell therapy offers new hope for the treatment of Alzheimer's disease.Frontiers in cell and developmental biology · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Yun Wei *Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, China.
Xinlei Du *Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, China.
Hongling GuoXiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, China.
Jingjing HanXiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, China.
Meixia LiuXiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, mitochondrial transfer has emerged as a universal phenomenon intertwined with various systemic physiological and pathological processes. Alzheimer's disease (AD) is a multifactorial disease, with mitochondrial dysfunction at its core. Although numerous studies have found evidence of mitochondrial transfer in AD models, the precise mechanisms remain unclear. Recent studies have revealed the dynamic transfer of mitochondria in Alzheimer's disease, not only between nerve cells and glial cells, but also between nerve cells and glial cells. In this review, we explore the pathways and mechanisms of mitochondrial transfer in Alzheimer's disease and how these transfer activities contribute to disease progression.

Indexed as

AD treatmentAlzheimer’s diseasemitochondrial dysfunctionmitochondrial transferneuroprotection

Identifiers

PMID39741520
PMCPMC11685155

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.